ArticleCell reports2024
A bacterial toxin co-opts caspase-3 to disable active gasdermin D and limit macrophage pyroptosis.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 20 citations in OpenAlex.
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Caspase-3/7 deficiency results in enhanced intestinal inflammation and reduced tumorigenesis.Science advances · 2026Article
- Structural basis and regulation of GSDME pore formation.Nature communications · 2026Article
- Interferon regulatory factor 5 involves the pathogenesis of emphysema through NLRP3 and Ly6C expressing cells.Experimental & molecular medicine · 2026Article
- Shaping death: how the microbiome regulates tumour cell demise and therapy response.Cancer metastasis reviews · 2026Review
- The landscape of regulated cell death: It's all downhill from here.Molecular cell · 2026Review
- Redefining Shiga toxin-induced human cell death as NLRP1- and gasdermin E-mediated pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Triptolide in Combination with the Gli1 Inhibitor GANT61 Eradicates Anaplastic Thyroid Cancer by Suppressing Cancer Stem Cell Self-Renewal and Enhancing Apoptosis and Pyroptosis.International journal of biological sciences · 2026Article
- Porcine cGAS-STING signalling induced apoptosis negatively regulates STING downstream IFN response and autophagy via different mechanisms.Virulence · 2025Article
- Regulation of inflammatory processes by caspases.Nature reviews. Molecular cell biology · 2025Review
- Article
- The Neglected Role of GSDMD C-Terminal in Counteracting Type I Interferon Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Etiopathogenesis of Kawasaki Disease: Evolving Understanding of Diverse Triggers.Immunity, inflammation and disease · 2025Review
- Article
- Coronavirus endoribonuclease antagonizes ZBP1-mediated necroptosis and delays multiple cell death pathways.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- Alcoholic brain injury is a modifiable risk factor: natural active substance intervention promises to improve alcohol-induced cognitive impairment.Frontiers in nutrition · 2025Review
- Mechanisms regulating host cell death duringmBio · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
During infections, host cells are exposed to pathogen-associated molecular patterns (PAMPs) and virulence factors that stimulate multiple signaling pathways that interact additively, synergistically, or antagonistically. The net effect of such higher-order interactions is a vital determinant of the outcome of host-pathogen interactions. Here, we demonstrate one such complex interplay between bacterial exotoxin- and PAMP-induced innate immune pathways. We show that two caspases activated during enterohemorrhagic Escherichia coli (EHEC) infection by lipopolysaccharide (LPS) and Shiga toxin (Stx) interact in a functionally antagonistic manner; cytosolic LPS-activated caspase-11 cleaves full-length gasdermin D (GSDMD), generating an active pore-forming N-terminal fragment (NT-GSDMD); subsequently, caspase-3 activated by EHEC Stx cleaves the caspase-11-generated NT-GSDMD to render it nonfunctional, thereby inhibiting pyroptosis and interleukin-1β maturation. Bacteria typically subvert inflammasomes by targeting upstream components such as NLR sensors or full-length GSDMD but not active NT-GSDMD. Thus, our findings uncover a distinct immune evasion strategy where a bacterial toxin disables active NT-GSDMD by co-opting caspase-3.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.